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Fig. 15.4 Schematic representation of a KNDy neuron depicting possible autoregulatory loops
and interactions with GnRH neurons
to present a unique GnRH pulse after every kisspeptin pulse. This possibility is in
keeping with the dense network of NKB fi bers surrounding KNDy neurons in the
ARC [ 25 , 30 , 33 ]. Next in this model, kisspeptin would reach the kisspeptin receptor
at the GnRH terminals to induce GnRH release to the median eminence. Of note,
there is no direct evidence of the presence of Kiss1r at the level of GnRH terminals;
however, this could be inferred based on the observations that (a) kisspeptin can
elicit GnRH secretion from explants of the mediobasal hypothalamus, which con-
tains few, if any, GnRH cell bodies [ 89 , 94 - 96 ] and (b) kisspeptin fi bers form close
appositions at the GnRH fi ber terminals [ 97 - 99 ]. At the same time, dynorphin (an
endogenous opioid peptide with known inhibitory action upon gonadotropin release
[ 100 , 101 ]), would act mainly on yet unknown intermediate neurons to eventually
shut down NKB and kisspeptin release, therefore creating a kisspeptin pulse.
Noteworthy, each neuropeptide released from KNDy neurons seems to target a dif-
ferent set of neurons. Thus, (a) kisspeptins act mainly on GnRH neurons, since
KNDy neurons themselves in the ARC are devoid of Kiss1 receptor [ 94 ] and do not
respond to kisspeptin [ 59 ]; (b) NKB seems to primarily activate KNDy neurons,
since GnRH neurons (at least in mice and sheep) do not express detectable levels of
NK3R [ 43 , 59 ]; (c) GnRH neurons do not express the dynorphin receptor (
κ
-opioid
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